Four grants were awarded for research that will increase our understanding of the causes, diagnosis, and treatment of CAPD, an umbrella term for a variety of disorders that affect the way the brain processes auditory information. All four of our CAPD grantees are General Grand Chapter Royal Arch Masons International award recipients.
+ Kenneth Vaden, Ph.D.
Medical University of South Carolina
Adaptive control of auditory representations in listeners with central auditory processing disorder
Central Auditory Processing Disorder (CAPD) is typically defined as impairment in the ability to listen and use auditory information because of atypical function within the central auditory system. The current study uses neuroimaging to characterize CAPD in older adults whose impaired auditory processing abilities could be driven by cognitive and hearing-related declines, in addition to differences in central auditory nervous system function. Functional neuroimaging experiments will be used to test the hypothesis that older adults with CAPD fail to benefit from top-down enhancement of auditory cortex representations for speech. In particular, activation of the adaptive control system in cingulo-opercular cortex is predicted to enhance speech representations in auditory cortex for normal listeners, but not to the same extent for older adults with CAPD. This project aims to develop methods to assess the quality of speech representations based on brain activity and characterize top-down control systems that interact with auditory cortex. The results of this study will improve our understanding of a specific top-down control mechanism, and examine when and how adaptive control enhances speech recognition for people with CAPD.
Research area: Speech Recognition; Neural Representations; Adaptive Control; Central Auditory Processing Disorder
Long term goal: The long term expected outcome from this line of research is to develop neural endophenotypes and methods to enhance characterization of CAPD. A control system that modulates auditory cortex activity could also provide a brain mechanism to guide future interventions.
Kenneth Vaden, Ph.D. earned his Ph.D. in Psychology at the University of CA, Irvine with dissertation research mentored by Dr. Greg S. Hickok, and his postdoctoral research was mentored by Dr. Mark A. Eckert at the Medical University of SC. As a Research Assistant Professor at the Medical University of SC, Dr. Vaden studies brain systems that support speech communication and how these change with age.
+ ANDREW DIMITRIJEVIC, PH.D.
Cincinnati Children's Hospital Medical Center
Sensory and Cognitive Processing in Children with Auditory Processing Disorders: Behavior and Electrophysiology
Central Auditory Processing Disorder (CAPD) can be defined as having a listening difficulty despite having normal hearing. One theory of CAPD is that this bottom-up processing isn’t working properly, a bit like listening to a de-tuned radio or TV. However, when the sound code reaches the cortex, it is mixed with a variety of signals from other systems, including vision, memory and attention. A second theory of CAPD is that the problem occurs at this level of mixing. In this ‘top-down’ theory, inappropriate control signals from high-level thinking systems, especially memory and attention, are thought to lead to misunderstanding of the code produced in the auditory system. Unfortunately, these two theories are difficult to tease apart. For example, a typical statement by a parent of a child with CAPD is that (s)he seems unaware when being spoken to. This could indicate poor listening due to inattention, or due to an inability to process speech sounds in the auditory system. Understanding which theory is correct may be important for treatment of CAPD. This research aims to tease apart these two theories by examining how the brain processes sound. One aspect of this research will examine how the brain encodes pitch and level fluctuations in sound. Both of these sound qualities are the “building blocks” of speech. If there are deficits at this level of neural processing then perhaps a “bottom up” or sound encoding problem exists. Another aspect of this research will examine a more cognitive approach and examine how the brain deals with speech in noise. This will be indexed by use of brain oscillations which are thought to reflect neural networks across different parts of the brain. Therefore by approaching CAPD from these two directions, it may be possible to show whether their listening difficulties are due to bottom-up or top-down processing problems.
Research Area: Electroencephalography, behavior, psychoacoustics, sensory processing, cognitive processing
Long term goal: This research addresses whether there are subtypes of Central Auditory Processing Disorder (CAPD), arising from deficits of bottom-up or top-down processing. Bottom-up processing refers to how the sound signal is encoded up to the level of the brain (i.e., ear to auditory nerve through the brainstem and up to the brain). Top-down processing is what the brain does with that information and includes cognition and attention. Understanding the mechanism of the CAPD will help direct clinicians as to what intervention may be most appropriate. For example, bottom-up problems may be best dealt with using a ‘communication device’. These resemble a cell phone ear piece and they are activated wirelessly by a small microphone worn by a teacher or parent. Top-down problems, on the other hand, may be better remedied by auditory training. Developing a test to tease apart these two scenarios and use this information to guide intervention is the long term goal of this project.
Andrew Dimitrijevic, Ph.D. received his Ph.D. at the University of Toronto working on auditory steady-state responses with Dr. Terrence Picton. He went on to do two postdoctoral fellowships, at University of British Columbia (with Dr. David Stapells) and at University of California Irvine (with Dr. Arnold Starr). He is currently at the Cincinnati Children’s Hospital and studies the electrophysiology of human hearing and development in children with auditory processing disorders, cochlear implants and single-sided deafness.
+ HARI BHARADWAJ, PH.D.
Massachusetts General Hospital
A systems approach to characterization of subcortical and cortical contributions to temporal processing deficits in central auditory processing disorders
Increasingly in the clinic, children report difficulty in understanding speech in the presence of other competing sounds. When these children are able to detect faint tones normally and show no classic signs of other neurological disorders, they are labeled as having Central Auditory Processing Disorder (CAPD). Understanding speech in a noisy setting is complex and relies both on the representation of subtle sound features by the auditory system, and the brain’s ability to make use of this information. Thus, difficulty can arise for a variety of reasons. Indeed, difficulty communicating in noisy settings is reported in a wide range of diagnostic categories such as Language Delays, Autism Spectrum Disorders, and Dyslexia among others. Yet, robust diagnostics that characterize CAPD – an auditory-specific disorder – as distinct from these other disorders are lacking. Here, we will use otoacoustic emissions and non-invasive brain imaging techniques (Electro/Magnetoencephalography) to passively measure how children’s inner ear, brainstem and cortex capture sound information. By examining the relationship between these measures and listening behavior, we aim to obtain a detailed objective test battery for the assessment of auditory function that would lead to novel clinical diagnostics for CAPD and provide clues for targeted intervention.
Research Area: Central Auditory Processing Disorders
Long term goal: This line of research seeks to achieve two parallel goals:
- To understand the physiological mechanisms that allow us to listen and communicate in noisy settings thereby illuminating why different groups of individuals have difficulty in such settings, and,
- To leverage this understanding to develop non-invasive objective tools that can be used in the diagnosis and stratification (“subtyping”) of a diverse yet overlapping setof communication disorders.
Hari Bharadwaj received his Ph.D. in Biomedical Engineering from Boston University and is currently a Research Fellow at Massachusetts General Hospital. Prior to that, he received his M.S. and B.Tech., both in Electrical Engineering, from University of Michigan and Indian Institute of Technology, respectively.
+ Beula Magimairaj, Ph.D.
University of Central Arkansas
Moving the science forward through interdisciplinary collaborative research integrating Hearing, Language, and Cognitive Science
Clinicians and researchers lack a consensual theoretical and clinical framework for conceptualizing Central Auditory Processing Disorder (CAPD) because professionals in different disciplines characterize it differently. Children diagnosed with CAPD may have deficits in attention, language, and memory, which often go unrecognized. There is a lack of a valid and reliable assessment tool that can characterize auditory processing, attention, language, and memory on the front-end. This project is an interdisciplinary effort to lay the foundation for such an assessment. Our goal is to develop an assessment that includes sensitive measures that can help build an initial profile of a child’s source(s) of difficulties that may be manifested as auditory processing deficits. During this 1-year project, computer-based behavioral tasks that integrate theoretical and methodological advances from the CAPD literature, and hearing, language, and cognitive science, will be developed. Tasks will be piloted on sixty typically developing children (7-11 years) who have no history of auditory processing/cognitive disorders for feasibility testing. Developing an assessment that will validly characterize the abilities of affected children is a multi-stage enterprise and this project is a critical first step.
Research Area: Central Auditory Processing Disorders
Long term goal: Clinicians lack a psychometrically sound assessment tool that can reliably characterize auditory processing and attention, language, and memory deficits that are known to frequently co-occur in children diagnosed with CAPD. Comprehensive assessment in all these areas is not feasible in a single assessment. In the long-term, the investigators aim to develop a sensitive and valid test that can serve as a front-end differential screening tool for children suspected to have CAPD. Guided by pilot data from the current project, future projects will extend the study to school-age children suspected to have CAPD. Future studies will establish test validity, reliability, normative data collection, and standardization. When developed, the assessment will serve as an important front-end tool for speech-language pathologists and audiologists for screening and for directing parents towards appropriate management resources. This preliminary testing can better inform further testing and possibly reduce misdiagnosis. Appropriate diagnosis of children suspected to have the complex condition known as CAPD, is the first step to providing helpful intervention. The development of a valid and reliable multi-disciplinary assessment will add to the growing research base regarding auditory function in children and how it relates to attention, memory, and language functioning.
Dr. Beula Magimairaj received a Ph.D. in Speech Language Science from Ohio University. She is also a clinically certified speech language pathologist. Dr. Magimairaj is currently Assistant Professor in Communication Sciences and Disorders at the University of Central Arkansas. Her research interests are in Specific Language Impairment and cognition, and include the study of children diagnosed with auditory processing disorders. Dr. Magimairaj's co-investigators on this grant are Dr. Natalie Benafield, Au.D. and Dr. Naveen Nagaraj, Ph.D., CCC-A.
Two grants were awarded that is focused on research (e.g., animal models, brain imaging, biomarkers, electrophysiology) that will increase our understanding of the mechanisms, causes, diagnosis, and treatments of hyperacusis and severe forms of loudness intolerance. Research that explores distinctions between hyperacusis and tinnitus is of special interest. Both of our Hyperacusis grants were funded by Hyperacusis Research.
+ Brad Buran, Ph.D.
Oregon Health & Science University
Neural mechanisms of hyperacusis in the inferior colliculus and cortex of ferrets with noise-induced auditory neurodegeneration
The development of effective treatments for hyperacusis (the diminished tolerance of loud sounds) and tinnitus (a persistent ringing in the ears) is limited by existing animal models. Current animal models are generated by high-intensity noise exposure or by the administration of salicylate, the active ingredient in aspirin. In addition to producing symptoms of hyperacusis and tinnitus, both of these manipulations lead to elevated hearing thresholds by damaging inner ear sensory cells. Damage to inner ear sensory cells leads to altered auditory processing, which makes it difficult to identify the specific changes that produce hyperacusis and tinnitus. While hearing loss is the primary risk factor for these disorders, they cannot be explained by damage to sensory cells alone. In fact, hyperacusis, tinnitus, and difficulty understanding speech in noise have been reported even in individuals with normal auditory thresholds. Therefore, in order to tease out the specific changes to the auditory system that result in tinnitus and hyperacusis, the ideal animal model should not have sensory cell damage.
Recent evidence from studies in mice suggests that moderate noise exposure can cause damage to the auditory nerve without altering hearing thresholds. Mice with this type of auditory nerve damage show symptoms of hyperacusis and humans who report tinnitus, but have normal auditory thresholds, also show signs of similar damage. It has also been hypothesized that auditory nerve damage will lead to increased difficulty understanding speech in the presence of background noise. Thus, moderate noise exposure provides a potential animal model for patients who have normal hearing thresholds, yet still experience hyperacusis, tinnitus, or difficulty hearing in noise. We will assess the perceptual effects of this auditory nerve damage by training noise-exposed ferrets to perform behavioral tests designed to parallel tests of hyperacusis, tinnitus, and difficulty hearing in noise that are conventionally used in human listeners. We will also assess how auditory responses in the central auditory system are altered by this type of auditory deficit to determine whether the changes in neural responses may explain the perceptual effects of hyperacusis, tinnitus, and difficulty hearing in noise.
Research Area: Hearing loss, auditory cortex plasticity, tinnitus, hyperacusis
Long term goal: To understand how hearing loss alters central auditory system function and how this abnormal function can be ameliorated to improve auditory outcomes.
Brad Buran completed a Ph.D. in the Harvard-MIT Program in Speech and Hearing Bioscience and Technology. He subsequently completed a postdoctoral fellowship at New York University with Dr. Dan Sanes, worked for Galenea, Corp. as a research scientist and is now a postdoctoral fellow in Dr. Stephen David’s laboratory in the Oregon Hearing Research Center at Oregon Health & Science University.
+ Kelly Radziwon, Ph.D.
SUNY University at Buffalo
The relationship between pain-associated proteins in the auditory pathway and hyperacusis
Hyperacusis is a condition in which sounds of moderate intensity are perceived as intolerably loud or even painful. Despite the apparent link between pain and hyperacusis in humans, little research has been conducted directly comparing the presence of inflammation along the auditory pathway and the occurrence of hyperacusis. One of the major factors limiting this research has been the lack of a reliable animal behavioral model of hyperacusis. However, using reaction time measurements as a marker for loudness perception, I have successfully assessed rats for drug-induced hyperacusis and, more recently, noise-induced hyperacusis. Briefly, the animals will be trained to detect noise bursts of varying intensity. As in humans, the rats will respond faster with increasing sound intensity. Following drug administration or noise exposure, rats will be deemed to have hyperacusis if they have faster-than-normal reaction times to moderate and high-level sounds. Therefore, the goal of the proposed research is to correlate the presence of pain-related molecules along the auditory pathway with reliable behavioral measures of drug and noise-induced hyperacusis.
Research Area: Hyperacusis; Hearing Loss
Long term goal: Since we have developed a reaction time paradigm that can reliably separate animals with hyperacusis from animals with loudness recruitment and normal loudness perception, we can now identify the biological correlates of this hearing disorder. Given that ear pain often co-occurs with hyperacusis, we felt that the most relevant biological markers of hyperacusis might be the expression of pain-related molecules found in the auditory system. Therefore, the long-term goals of this project are to determine the relationship between pain-related molecules and inflammation along the auditory pathway and the perceptual experience of hyperacusis. We will start by focusing on three molecules, SP, NK1, and TRPV1, but will adjust our biochemical analysis depending upon the results of this project. However, if these molecules are correlated with hyperacusis, then this will provide the biological markers needed for the development of treatments for ear pain and hyperacusis.
Kelly Radziwon, Ph.D. received her Ph.D. in Cognitive Psychology from the University at Buffalo, SUNY in 2013. Currently, she is a post-doctoral fellow in Dr. Richard Salvi’s lab in the Center for Hearing and Deafness at the University at Buffalo. Dr. Radziwon’s research interests include animal psychoacoustics as it relates to hearing loss, tinnitus, and hyperacusis.
Two grants were awarded for innovative research that will increase our understanding of the inner ear and balance disorder Ménière’s disease.
+ Wafaa Kaf, M.D., MS.c., Ph.D.
Missouri State University
Novel Ménière’s disease diagnosis: extratympanic simultaneous recording of ECochG and ABR to fast click rates using CLAD technique
Ménière’s disease is mainly diagnosed clinically with no available sensitive objective measures to confirm clinical diagnosis. Current auditory electrophysiologic measures such as standard electrocochleography (ECochG) to a slow click rate has low sensitivity that limits its clinical use. Also, standard ECochG to slow rate cannot measure neural adaptation phenomenon (decrease in the neural firing between the inner hair cells and auditory nerve) that occurs in response to continuous presentation of a fast acoustic stimulus. Although other technique modifications of ECochG such as maximum length sequence to fast rate seem to be promising, several limitations in extracting responses to very fast rates exist with this measure that hinder their clinical use for detection of Ménière’s disease. The new continuous loop averaging deconvolution (CLAD) algorithm is a promising technique to extract overlapping auditory evoked responses to very fast rates, providing valuable information about cochlear and neural function of clinical populations. Thus, the use of CLAD with fast rate ECochG and auditory brainstem response (ABR) has the potential to detect early Ménière’s disease by studying the neural adaptation phenomenon. It is hypothesized that Ménière’s disease may show abnormally fast neural adaptation that may manifest as fast degradation of AP and ABR response amplitudes and prolongation of latency as a function of click rate. The current objectives and the long-term goals of this project are to establish and advance ECochG and ABR measures using CLAD technique to identify the critical rate at which neural adaptation starts as a marker for early diagnosis, differential diagnosis and classification of Ménière’s disease.
Research Area: Ménière’s Disease
Long term goal: This study and consequent studies will support clinical diagnosis and improve our understanding of the pathophysiology of the disease process. Findings from this project will lead to a series of clinical studies to 1) evaluate neural adaptation phenomenon in early versus late phases of Ménière’s disease as well as unilateral versus bilateral cases, 2) improve the understanding of the pathophysiology and the fluctuation of Ménière’s disease by comparing pattern and critical point of neural adaptation during and following Meniere’s attacks; 3) compare pattern and critical point of neural adaptation among Ménière’s patients of different clinical classification: possible vs. probable, vs. definite vs. certain; 4) distinguish Ménière’s disease from other related pathologies such as migraine associated vertigo, semicircular canal dehiscence and acoustic neuroma, 5) study adaptation phenomenon to tone burst stimuli versus click stimuli for more accurate diagnosis of Ménière’s disease; and 6) monitor the effect of treatment by comparing critical rate of neural adaptation before and after treatment.
Wafaa Kaf, M.D., MS.c., Ph.D., is a professor of Audiology at MSU. Dr. Kaf’s influences in auditory neurophysiology research have been shaped by several education as well as research and medical training experiences. Her research is primarily focused on evaluating neurophysiological correlates of normal and abnormal auditory processing to assess hearing thresholds, neural adaptation of the inner ear and auditory brainstem, and the auditory efferent function. Dr. Kaf has several national and international research presentations on these topics.
Dr. Kaf's grant is funded by The Estate of Howard F. Schum.
+ Frances Meredith, Ph.D.
University of Colorado Denver
The role of K+ conductances in coding vestibular afferent responses
Approximately 615,000 people in the United States suffer from Meniere’s disease, a disorder of the inner ear that causes episodic vertigo, tinnitus and progressive hearing loss. The underlying etiology of the disease is not known but may include defects in ion channels and alterations in inner ear fluid potassium (K+) ion concentration. Specialized hair cells inside the ear detect head movement in the vestibular system and sound signals in the cochlea. A rich variety of channels is found on the membranes of hair cells as well as on the afferent nerve endings that form connections (synapses) with hair cells. Many of these channels selectively allow the passage of K+ ions and are thought to be important for maintaining the appropriate balance of K+ ions in inner ear fluids. I study an unusual type of nerve ending called a calyx, found at the ends of afferent nerves that form synapses with type I hair cells of the vestibular system. These nerves send electrical signals to the brain about head movements. My goal is to use immunocytochemistry and electrophysiology to identity K+ channels on the calyx membrane and to explore their role in regulating electrical activity and K+ levels in inner ear fluid. I will identify potential routes for K+ entry that could influence calyx properties. I will investigate whether altered ionic concentrations in inner ear fluid change the buffering capacity of K+ channels and whether this affects the signals that travel along the afferent vestibular nerve to the brain. Meniere’s disease is a disorder of the entire membranous labyrinth of the inner ear and thus affects both the vestibular sensory organs and the cochlea. Similar K+ ion channels are expressed in vestibular and auditory afferent neurons. Studying ion channels present in both auditory and vestibular systems will reveal properties common to both systems and will increase our understanding of the importance of ion channels in Meniere’s disease.
Research Area: Ménière’s Disease
Long term goal: The long term goals of my research are to find out whether expression of ion channels varies in calyces innervating different regions of the vestibular sensory epithelium and to explore the roles that ion channels play in shaping electrical signals carried to the brain. It is important to understand the basic functioning of ion channels: knowledge of their role in sensory coding and knowing how their expression varies regionally may contribute to the design of effective technologies, e.g. cochlear and vestibular implants, to mitigate the effects of inner ear disorders. In addition, linking ion channel deficits to pathology of the inner ear may enable us to treat vestibular and auditory symptoms using ion channel modulators.
Frances Meredith, Ph.D. received her Ph.D. in Neuroscience from the University of Colorado, Anschutz Medical Campus, in 2012. She is now in her third postdoctoral year in Dr. Katherine Rennie’s laboratory in the Department of Otolaryngology at the University of Colorado.
Dr. Meredith's grant is funded by William Randolph Hearst Foundation through their William Randolph Hearst Endowed Otologic Fellowship.
Two grants were awarded for innovative research that will increase our understanding of the mechanisms, causes, diagnosis, and treatment of tinnitus.
+ Xiping Zhan, Ph.D.
Dopaminergic activity in modulation of noise-induced tinnitus
Tinnitus is a major challenge for public health because it is a condition that is associated with hearing loss and can contribute to debilitating emotional stress, anxiety, and mental fatigue. Dr. Zhan’s interest is focused on the mechanisms that generate tinnitus and modulate tinnitus associated anxiety and depression using an animal model. His studies focus on dopaminergic activity in the limbic midbrain. Dopamine and its receptors play an important role in human mood behavior. Recently, dopamine has been suggested to be involved in tinnitus. Dr. Zhan’s research is designed to find out how dopamine neurons are communicating with other neurons to contribute to tinnitus generation. In addition, he also investigates how the functions of dopamine cells are modified during the development of tinnitus following noise exposures. These studies will shed light on the cellular mechanisms of tinnitus and offer a novel avenue for drug therapy.
Research Area: Tinnitus and associated distress
Long term goal: Tinnitus is a common disease stemming from plastic changes or synaptic reorganization often caused by hearing loss, acoustic trauma and ototoxic drugs. This disorder is associated with distress and depression. The limbic circuits are implicated to be involved, but it is still elusive how a specific pathway is involved. Therefore, the long term goals of this research are to decipher the underpinnings for tinnitus and associated mental disorders with emphasis on the dopaminergic pathways and functions.
In summary, we will be able elucidate new knowledge about the role of dopaminergic activity in tinnitus and associated distress. This will guide us to establish a protocol by taking advantage of psychiatric drugs, such as dopaminergic active drugs, to alleviate the symptoms caused by tinnitus and the associated distress. It may also help us to develop novel drugs and manage tinnitus with more effective intervention. Further more, it may help physicians to formulate new guidelines for tinnitus suffers to manage negative emotions caused by tinnitus.
Dr. Zhan obtained his Ph.D. in the College of Life Sciences, East China Normal University, Shanghai, 1999. He completed his postdoctoral work on the function of the cochlear nucleus granule cell domain at Johns Hopkins University (2006), and tinnitus modulation at Georgetown University (2009). In 2014, he became a research assistant professor in the Department of Physiology, College of Medicine at Howard University, Washington, DC.
+ Noah R. Druckenbrod , Ph.D.
Identifying roles for contact-dependent signaling between neurons and glia during axon guidance and synaptic targeting
The mature cochlea is a spiraled hollow chamber of bone that contains all the necessary components to transmit sound information to the brain. This feat is accomplished by the precise arrangement of hair cells and spiral ganglion neurons (SGNs). This arrangement requires SGNs extend peripheral projections and establish precise synaptic connections with hair cells. What signals guide these axons through the three-dimensional terrain of the cochlea? Most studies focus on the roles of classically described axon guidance cues, which act over long distances to attract or repel axons. However, mounting evidence from recent studies and our own preliminary data lead us to hypothesize that contact-dependent signaling between SGNs and Schwann cells (SCs) are required for normal development of inner ear neural architecture and hearing. The precise role of contact-dependent interactions between SGN axons and SCs on auditory circuit formation remains unknown. This is due in part to the obstacles towards gathering high-resolution, time-lapsed information on the spatial relationships between SGNs and SCs in situ. Therefore, we will genetically label and characterize live cellular interactions between these cells in their normal, and then abnormal, physiological environment. We will measure the extent to which each of these cell types rely on each other for normal migration, differentiation, proliferation and survival. Because we have identified a mutant in which SGN-Schwann cell interaction appears disrupted, these studies will also provide insight to our understanding of Schwannoma formation. Schwannomas are Schwann cell tumors commonly found in the inner-ear and are thought to arise from a disruption in reciprocal signaling between spiral ganglion neurons (SGNs) and Schwann cells. As these tumors grow they compress afferent vestibular and auditory nerves, usually causing hearing loss, tinnitus, and dizziness. Therefore, these studies will not only contribute to our understanding of auditory circuit formation but also provide insight into what can go wrong when SGN-Schwann cell interaction is disrupted.
Research Area: Hearing Loss, Tinnitus, Neuron-glia interaction, auditory circuit development and regeneration
Long term goal: Currently very little is known the interaction between SGNs and glia during development and disease. Completion of the proposed experiments will be the first ever to show live interaction between neurites and peripheral glia during axon guidance and synaptic targeting in any mammalian system. Upon completion of the pilot experiments in this proposal, we will have determined whether SGN wiring is regulated by contact-dependent interactions with developing Schwann cells. Furthermore, it will determine whether disrupted interaction between these two cell types leads to disorganized auditory wiring (deafness), and abnormal Schwann cell proliferation or differentiation. It is my hope to eventually use the methods of this proposal as a platform to bridge the gap between the analysis provided by whole-organ time-lapse microscopy and the macroscopic phenotype of experimental animals, and, eventually, of neurological patients.
Noah Druckenbrod first did research on adrenergic receptor trafficking under Dr. Mike Sievert and Dr. Arnold Ruoho in the department of Pharmacology through an undergraduate honors thesis program in Neurobiology. Later he received his Ph.D. working on the molecular and cellular biology of enteric nervous system development and disease with Dr. Miles Epstein at the University of Wisconsin in Madison. Dr. Druckenbrod is currently a postdoctoral research fellow with Dr. Lisa Goodrich’s laboratory in the department of Neurobiology at Harvard Medical School.
Dr. Druckenbrod's grant was generously funded by The Barbara Epstein Foundation, Inc.